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BMJ Clinical Evidence Oct 2007Up to 40% of adults have insomnia, with difficulty getting to sleep, early waking, or feeling unrefreshed on waking. The prevalence of insomnia increases with age. Other... (Review)
Review
INTRODUCTION
Up to 40% of adults have insomnia, with difficulty getting to sleep, early waking, or feeling unrefreshed on waking. The prevalence of insomnia increases with age. Other risk factors include psychological factors, stress, daytime napping, and hyperarousal.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of non-drug treatments for insomnia in elderly people? What are the effects of drug treatments for insomnia in elderly people? We searched: Medline, Embase, The Cochrane Library and other important databases up to October 2006 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found 28 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review we present information relating to the effectiveness and safety of the following interventions: benzodiazepines (brotizolam, flurazepam, loprazolam, midazolam, nitrazepam, quazepam, temazepam, and triazolam), cognitive behavioural therapy, diphenhydramine, exercise programmes, timed exposure to bright light, zaleplon, zolpidem, and zopiclone.
Topics: Aged; Cognitive Behavioral Therapy; Flurazepam; Humans; Risk Factors; Sleep; Sleep Initiation and Maintenance Disorders; Temazepam
PubMed: 19450355
DOI: No ID Found -
Frontiers in Physiology 2021Fatigue poses an important safety risk to civil and military aviation. In addition to decreasing performance in-flight (chronic) fatigue has negative long-term health... (Review)
Review
Fatigue poses an important safety risk to civil and military aviation. In addition to decreasing performance in-flight (chronic) fatigue has negative long-term health effects. Possible causes of fatigue include sleep loss, extended time awake, circadian phase irregularities and work load. Despite regulations limiting flight time and enabling optimal rostering, fatigue cannot be prevented completely. Especially in military operations, where limits may be extended due to operational necessities, it is impossible to rely solely on regulations to prevent fatigue. Fatigue management, consisting of preventive strategies and operational countermeasures, such as pre-flight naps and pharmaceuticals that either promote adequate sleep (hypnotics or chronobiotics) or enhance performance (stimulants), may be required to mitigate fatigue in challenging (military) aviation operations. This review describes the pathophysiology, epidemiology and effects of fatigue and its impact on aviation, as well as several aspects of fatigue management and recommendations for future research in this field.
PubMed: 34552504
DOI: 10.3389/fphys.2021.712628 -
Anaesthesia Nov 1997
Topics: Administration, Oral; Child; Humans; Hypnotics and Sedatives; Midazolam; Premedication
PubMed: 9404195
DOI: No ID Found -
British Medical Journal May 1980
Topics: Adult; Aged; Anti-Anxiety Agents; Chlormethiazole; Humans; Motor Skills; Posture; Temazepam; Wakefulness
PubMed: 6104531
DOI: 10.1136/bmj.280.6227.1322-b -
British Medical Journal Apr 1980
Topics: Anti-Anxiety Agents; Chlormethiazole; Half-Life; Humans; Motor Activity; Temazepam
PubMed: 6104528
DOI: 10.1136/bmj.280.6221.1085-c -
British Medical Journal Mar 1980
Topics: Anti-Anxiety Agents; Chlormethiazole; Humans; Mental Processes; Sleep; Temazepam
PubMed: 6102879
DOI: 10.1136/bmj.280.6217.860-b -
The Cochrane Database of Systematic... Jul 2014Post-traumatic stress disorder (PTSD) is a debilitating disorder which, after a sufficient delay, may be diagnosed amongst individuals who respond with intense fear,... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Post-traumatic stress disorder (PTSD) is a debilitating disorder which, after a sufficient delay, may be diagnosed amongst individuals who respond with intense fear, helplessness or horror to traumatic events. There is some evidence that the use of pharmacological interventions immediately after exposure to trauma may reduce the risk of developing of PTSD.
OBJECTIVES
To assess the effects of pharmacological interventions for the prevention of PTSD in adults following exposure to a traumatic event.
SEARCH METHODS
We searched the Cochrane Depression, Anxiety and Neurosis Controlled Trials Register (CCDANCTR-Studies and CCDANCTR-References) (to 14 February 2014). This register contains relevant reports of randomised controlled trials from the following bibliographic databases: CENTRAL (all years); EMBASE (1974 to date); MEDLINE (1950 to date) and PsycINFO (1967 to date). We identified unpublished trials by searching the National Institute of Health (NIH) Reporter, the metaRegister of Controlled Trials database (mRCT) and the WHO International Clinical Trials Registry Platform (to December 2013). We scanned the reference lists of articles for additional studies. We placed no constraints on language and setting.
SELECTION CRITERIA
We restricted studies to randomised controlled trials (RCTs) of pharmacological interventions compared with placebo for the prevention of PTSD in adults.
DATA COLLECTION AND ANALYSIS
Two authors (TA and JI) independently assessed trials for eligibility and inclusion based on the review selection criteria. We independently extracted sample, methodological, outcome and 'Risk of bias' data, as well as the number of side effects, from each trial and entered these into a customised data extraction form. We contacted investigators for missing information. We calculated summary statistics for continuous and dichotomous variables (if provided). We did not undertake subgroup analyses due to the small number of included studies.
MAIN RESULTS
We included nine short-term RCTs (duration 12 weeks or less) in the analysis (345 participants; age range 18 to 76 years). Participants were exposed to a variety of traumas, ranging from assault, traffic accidents and work accidents to cardiac surgery and septic shock. Seven studies were conducted at single centres. The seven RCTs included four hydrocortisone studies, three propranolol studies (of which one study had a third arm investigating gabapentin), and single trials of escitalopram and temazepam. Outcome assessment measures included the Clinician-Administered PTSD Scale (CAPS), the 36-Item Short-Form Health Survey (SF-36) and the Center for Epidemiological Studies - Depression Scale (CES-D).In four trials with 165 participants there was moderate quality evidence for the efficacy of hydrocortisone in preventing the onset of PTSD (risk ratio (RR) 0.17; 95% confidence interval (CI) 0.05 to 0.56; P value = 0.004), indicating that between seven and 13 patients would need to be treated with this agent in order to prevent the onset of PTSD in one patient. There was low quality evidence for preventing the onset of PTSD in three trials with 118 participants treated with propranolol (RR 0.62; 95% CI 0.24 to 1.59; P value = 0.32). Drop-outs due to treatment-emergent side effects, where reported, were low for all of the agents tested. Three of the four RCTs of hydrocortisone reported that medication was more effective than placebo in reducing PTSD symptoms after a median of 4.5 months after the event. None of the single trials of escitalopram, temazepam and gabapentin demonstrated evidence that medication was superior to placebo in preventing the onset of PTSD.Seven of the included RCTs were at a high risk of bias. Differential drop-outs between groups undermined the results of three studies, while one study failed to describe how the allocation of medication was concealed. Other forms of bias that might have influenced study results included possible confounding through group differences in concurrent medication and termination of the study based on treatment response.
AUTHORS' CONCLUSIONS
There is moderate quality evidence for the efficacy of hydrocortisone for the prevention of PTSD development in adults. We found no evidence to support the efficacy of propranolol, escitalopram, temazepam and gabapentin in preventing PTSD onset. The findings, however, are based on a few small studies with multiple limitations. Further research is necessary in order to determine the efficacy of pharmacotherapy in preventing PTSD and to identify potential moderators of treatment effect.
Topics: Adrenergic beta-1 Receptor Antagonists; Adult; Aged; Amines; Anti-Anxiety Agents; Anti-Inflammatory Agents; Antidepressive Agents, Second-Generation; Citalopram; Cyclohexanecarboxylic Acids; Gabapentin; Humans; Hydrocortisone; Middle Aged; Propranolol; Randomized Controlled Trials as Topic; Stress Disorders, Post-Traumatic; Temazepam; Young Adult; gamma-Aminobutyric Acid
PubMed: 25001071
DOI: 10.1002/14651858.CD006239.pub2 -
Drugs in R&D Mar 2022Urine is conventionally used as a specimen to document diazepam-related crimes; however, few reports have described the pharmacokinetics of diazepam and its metabolites...
BACKGROUND
Urine is conventionally used as a specimen to document diazepam-related crimes; however, few reports have described the pharmacokinetics of diazepam and its metabolites in urine.
OBJECTIVE
This study aimed to investigate the pharmacokinetics of diazepam and its metabolites, including glucuronide compounds, in the urine of Chinese participants.
METHODS
A total of 28 volunteers were recruited and each participant ingested 5 mg of diazepam orally. Ten milliliters of urine were collected from each participant at post-consumption timepoints of prior (zero), 1, 2, 4, 8, 12, and 24 h and 2, 3, 6, 12, and 15 days. All samples were extracted by solid-phase extraction and analyzed using high-performance liquid chromatography-tandem mass spectrometry. Diazepam and its main metabolites, except for temazepam, were detected in the urine of volunteers. Pharmacokinetic parameters were analyzed using the pharmacokinetic software DAS according to the non-compartment model.
RESULTS
Urinary diazepam peaked at 2.38 ng/mL (C) and 1.93 h (T). The urinary metabolite nordiazepam peaked at 1.17 ng/mL and 100.21 h; temazepam glucuronide (TG) peaked at 145.61 ng/mL and 41.14 h; and oxazepam glucuronide (OG) peaked at 101.57 ng/mL and 165.86 h. The elimination half-life (t) and clearance (CLz/F) for diazepam were 119.58 h and 65.77 L/h, respectively. The t of the metabolites nordiazepam, TG, and OG was 310.58 h, 200.17 h, and 536.44 h, respectively. Finally, this study found that both diazepam and its main metabolites in urine were detectable for at least 15 days, although there were individual differences.
CONCLUSION
The results regarding diazepam pharmacokinetics in urine would be of great help in forensic science and drug screening.
Topics: China; Chromatography, High Pressure Liquid; Diazepam; Humans; Nordazepam; Solid Phase Extraction
PubMed: 35099786
DOI: 10.1007/s40268-021-00375-y -
Drug Safety - Case Reports Dec 2015Clozapine is used for decennia for the treatment of schizophrenia. Agranulocytosis, diabetic ketoacidosis, gastrointestinal hypomotility, and myocarditis are well-known...
CONTEXT
Clozapine is used for decennia for the treatment of schizophrenia. Agranulocytosis, diabetic ketoacidosis, gastrointestinal hypomotility, and myocarditis are well-known adverse effects of clozapine, which are sometimes life threatening. Here we report a case of rhabdomyolysis upon an acute overdose of clozapine.
CASE
A male patient, 36 years, with elevated creatinine kinase levels (9899 U/l), developed rhabdomyolysis afterafter admission to the emergency department. Approximately 2-4 h earlier he had intoxicated himself with his maintenance oral medication clozapine 125 mg, temazepam 20 mg and lorazepam 1.5 mg. Co-medications, and physical and laboratory examinations did not reveal other risk factors for rhabdomyolysis. According to the Naranjo probability scale there was a probable relation between clozapine dose and symptoms, that developed approximately 2-4 h after the auto-intoxication of 125 mg tablets. At day 5 of hospitalization, clozapine and creatinine kinase levels returned to normal and the patient was discharged with no somatic sequelae.
CONCLUSIONS
Elevated creatinine kinase levels in acute clozapine intoxication may be an indicator that rhabdomyolysis may be involved.
PubMed: 27747721
DOI: 10.1007/s40800-015-0011-7 -
British Journal of Clinical Pharmacology 19791 The effect of temazepam 15 and 30 mg, flurazepam 15 and 30 mg, quinalbarbitone 100 and 200 mg and placebo were studied in 14 healthy male volunteers according to a... (Clinical Trial)
Clinical Trial
1 The effect of temazepam 15 and 30 mg, flurazepam 15 and 30 mg, quinalbarbitone 100 and 200 mg and placebo were studied in 14 healthy male volunteers according to a Latin-square design. At 14-d intervals subjects received capsules 30 min before bedtime on 2 consecutive nights and were evaluated for objective sleep characteristics, for morning estimates of sleep characteristics, and for cognitive and psychomotive performance and subjective state at 3.5, 10.0 and 22.5 h after ingestion. 2 Changes in sleep induction and sleep maintenance were observed with temazepam 30 mg and flurazepam 30 mg had the greater effect on cognitive performance, whereas quinalbarbitone 20 mg had the greater effect on psychomotive performance. Subjective assessments of alertness were most affected by flurazepam, and by quinalbarbitone 200 mg. 4 The results suggest that temazepam produces less residual effects and is shorter acting than quinalbarbitone and flurazepam.
Topics: Adult; Anti-Anxiety Agents; Cognition; Emotions; Flurazepam; Humans; Male; Memory; Motor Skills; Secobarbital; Sleep; Sleep, REM; Temazepam
PubMed: 41542
DOI: 10.1111/j.1365-2125.1979.tb00456.x